The intravenous injection of F1 hybrid mice with parental T cells result in a loss in the ability of the F1 mice to generate T-cell mediated immune responses in vitro to graft-versus-host immune deficiency (GVHID). Recognition of host class II MHC antigens by donor cells is required to initiate GVHID. Recognition of host class I MHC antigens doesn't induce GVHID. Recognition of class II only results in loss of self + X responses but not of allogeneic responses; recognition of class I and II results in loss of self + X and allogeneic responses. Induction of GVHID by class I and II recognition requires both L3T4+ and Lyt2+ cells; induction of GVHID by class II only recognition requires only L3T4+ parental T cells. GVHID is accompanied by loss of ability to produce IL 2 and in loss of expression of IL 2 receptors. This IL 2 loss was observed in both class I and II and class II only GVHID. Recovery of immune function from GVHID was preceded by recovery of IL 2 receptor expression and IL 2 production. GVHID was used to abrogate natural resistance to bone marrow grafts in F1 hybrid mice.